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Population
Mice
Comparison
STIM1 ablation vs intact STIM1 in exercise-induced physiological cardiac hypertrophy
Design
Animal experimental study
SOCE inhibition may blunt exercise-induced cardiac adaptations; leaves open its role as a shared therapeutic target in human hypertrophy.
entry (SOCE) has been implicated in pathological cardiac hypertrophy; however, its role in physiological hypertrophy is unknown. Here we report that SOCE is also essential for physiological cardiac hypertrophy and functional adaptations in response to endurance exercise. These adaptations were associated with activation of AKT/mTOR pathway and curtailed cardiac autophagy and degeneration. Thus, SOCE is a common mechanism and an important bifurcation point for signaling paths involved in physiological and pathological hypertrophy.
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Bonilla et al. (2023) studied this question.
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